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Editorial
July 2017

Linking Amyloid-β and Tau Deposition in Alzheimer Disease

Author Affiliations
  • 1Department of Radiology, Mayo Clinic, Rochester, Minnesota
  • 2Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden
  • 3Department of Psychiatry and Neurochemistry, University of Gothenburg, Gothenburg, Sweden
  • 4Clinical Memory Research Unit, Lund University, Lund, Sweden
JAMA Neurol. 2017;74(7):766-768. doi:10.1001/jamaneurol.2017.0323

Deposition of abnormal or misfolded proteins, amyloid-β (Aβ) into plaques and hyperphosphorylated tau as paired helical filaments and eventually neurofibrillary tangles, is the hallmark of Alzheimer disease (AD). Until the beginning of this century, mechanistic inferences into the progression of AD were mainly based on autopsy data. The emergence of amyloid imaging has significantly improved our understanding of the disease processes. Numerous amyloid imaging studies have confirmed autopsy findings that Aβ accumulation may be one of the earliest changes associated with AD. Amyloid imaging has further been proposed as a tool for the identification of individuals with preclinical AD and for identifying the pathologic cause of symptoms underlying mild cognitive impairment and dementia in research studies.1,2 The availability of Aβ imaging has also aided ongoing clinical trials that are focused on targeting Aβ and its clearance.

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